Foxc1 and Foxc2 in the Neural Crest Are Required for Ocular Anterior Segment Development
Identifieur interne : 000543 ( Main/Curation ); précédent : 000542; suivant : 000544Foxc1 and Foxc2 in the Neural Crest Are Required for Ocular Anterior Segment Development
Auteurs : Seungwoon Seo [États-Unis, Corée du Sud] ; Lisheng Chen [États-Unis] ; Wenzhong Liu [États-Unis] ; Demin Zhao [États-Unis] ; Kathryn M. Schultz [États-Unis] ; Amy Sasman [États-Unis] ; Ting Liu [États-Unis] ; Hao F. Zhang [États-Unis] ; Philip J. Gage [États-Unis] ; Tsutomu Kume [États-Unis]Source :
- Investigative Ophthalmology & Visual Science [ 0146-0404 ] ; 2017.
Abstract
The large Forkhead (Fox) transcription factor family has essential roles in development, and mutations cause a wide range of ocular and nonocular disease. One member,
To specifically delete
Neural crest-
The neural crest-
Url:
DOI: 10.1167/iovs.16-21217
PubMed: 28253399
PubMed Central: 5361455
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Liu, Ting" sort="Liu, Ting" uniqKey="Liu T" first="Ting" last="Liu">Ting Liu</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Zhang, Hao F" sort="Zhang, Hao F" uniqKey="Zhang H" first="Hao F." last="Zhang">Hao F. Zhang</name>
<affiliation wicri:level="2"><nlm:aff id="aff4">Department of Biomedical Engineering, Northwestern University, Evanston, Illinois, United States</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Biomedical Engineering, Northwestern University, Evanston, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
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<author><name sortKey="Gage, Philip J" sort="Gage, Philip J" uniqKey="Gage P" first="Philip J." last="Gage">Philip J. Gage</name>
<affiliation wicri:level="2"><nlm:aff id="aff3">Department of Ophthalmology and Visual Science, University of Michigan, Ann Arbor, Michigan, United States</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Ophthalmology and Visual Science, University of Michigan, Ann Arbor, Michigan</wicri:regionArea>
<placeName><region type="state">Michigan</region>
</placeName>
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<author><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name>
<affiliation wicri:level="2"><nlm:aff id="aff1">Feinberg Cardiovascular Research Institute, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Feinberg Cardiovascular Research Institute, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
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<series><title level="j">Investigative Ophthalmology & Visual Science</title>
<idno type="ISSN">0146-0404</idno>
<idno type="eISSN">1552-5783</idno>
<imprint><date when="2017">2017</date>
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<front><div type="abstract" xml:lang="en"><sec id="st1"><title>Purpose</title>
<p>The large Forkhead (Fox) transcription factor family has essential roles in development, and mutations cause a wide range of ocular and nonocular disease. One member, <italic>Foxc2</italic>
is expressed in neural crest (NC)-derived periocular mesenchymal cells of the developing murine eye; however, its precise role in the development, establishment, and maintenance of the ocular surface has yet to be investigated.</p>
</sec>
<sec id="st2"><title>Methods</title>
<p>To specifically delete <italic>Foxc2</italic>
from NC-derived cells, conditional knockout mice for <italic>Foxc2</italic>
(NC-<italic>Foxc2</italic>
<sup>−</sup>
<italic><sup>/</sup>
</italic>
<sup>−</sup>
) were generated by crossing <italic>Foxc2<sup>F</sup>
</italic>
mice with <italic>Wnt1-Cre</italic>
mice. Similarly, we also generated compound NC-specific mutations of <italic>Foxc2</italic>
and a closely related gene, <italic>Foxc1</italic>
(NC-<italic>Foxc1</italic>
<sup>−</sup>
<italic><sup>/</sup>
</italic>
<sup>−</sup>
;NC-<italic>Foxc2</italic>
<sup>−</sup>
<italic><sup>/</sup>
</italic>
<sup>−</sup>
) in mice.</p>
</sec>
<sec id="st3"><title>Results</title>
<p>Neural crest-<italic>Foxc2</italic>
<sup>−</sup>
<italic><sup>/</sup>
</italic>
<sup>−</sup>
mice show abnormal thickness in the peripheral-to-central corneal stroma and limbus and displaced pupils with irregular iris. The neural crest-specific mutation in <italic>Foxc2</italic>
also leads to ectopic neovascularization in the cornea, as well as impaired ocular epithelial cell identity and corneal conjunctivalization. Compound, NC-specific <italic>Foxc1</italic>
; <italic>Foxc2</italic>
homozygous mutant mice have more severe defects in structures of the ocular surface, such as the cornea and eyelids, accompanied by significant declines in the expression of another key developmental factor, Pitx2, and its downstream effector Dkk2, which antagonizes canonical Wnt signaling.</p>
</sec>
<sec id="st4"><title>Conclusions</title>
<p>The neural crest-<italic>Foxc2</italic>
mutation is associated with corneal conjunctivalization, ectopic corneal neovascularization, and disrupted ocular epithelial cell identity. Furthermore, Foxc2 and Foxc1 cooperatively function in NC-derived mesenchymal cells to ensure proper morphogenesis of the ocular surface via the regulation of Wnt signaling. Together, Foxc2 is required in the NC lineage for mesenchymal-epithelial interactions in corneal and ocular surface development.</p>
</sec>
</div>
</front>
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